Seborrhoeic Dermatitis
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Direct answer
Greasy, yellow-white scale sitting precisely where sebum flows — the scalp as dandruff, the nasolabial folds, eyebrows, glabella, central chest and skin folds — defines seborrhoeic dermatitis, an inflammatory reaction to Malassezia yeasts rather than a classical infection: yeast lipases liberate fatty acids that irritate susceptible skin. First-line treatment is ketoconazole 2% shampoo used on scalp and face twice weekly until clear, then weekly for maintenance, with short courses of mild topical corticosteroid or a topical calcineurin inhibitor for inflamed facial flares. The disease relapses whenever treatment stops — maintenance counselling is part of the prescription. Severe, refractory or atypical presentations should prompt HIV testing and screening for Parkinson disease; infancy brings the self-limiting cradle cap.
What you must remember
- Distribution is the diagnosis: sebum-rich terrain — scalp, nasolabial folds, eyebrows, beard area, glabella, presternal chest, axillary and inguinal folds; margin sharply demarcated with greasy scale on dull erythema.
- Mechanism: Malassezia (globosa and restricta) colonises everyone, but lipase-released free fatty acids ignite inflammation only in susceptible hosts — hence antifungals help though the yeast is not an invader.
- Treatment ladder: ketoconazole 2% shampoo or ciclopirox twice weekly for two to four weeks, then weekly-to-fortnightly maintenance; mild topical steroid (hydrocortisone 1%, or mometasone briefly) for flares; tacrolimus or pimecrolimus for steroid-sparing facial control; oral itraconazole for severe disease.
- Infancy: cradle cap — yellowish scale over the vertex with self-resolution; emollients and dilute ketoconazole shampoo suffice; avoid potent steroids.
- The two associations worth marks: HIV (severe, extensive, treatment-recalcitrant seborrhoeic dermatitis is an indicator to offer testing) and Parkinson disease (striking seborrhoea years before or after diagnosis); spinal cord injury adds a third, weaker link.
- Maintenance truth: relapse follows cessation within weeks to months in most patients — schedule the maintenance day rather than promising cure.
- Differential anchors: psoriasis (well-demarcated extensor plaques, elbow-knee symmetry, nail pitting), tinea (KOH-positive, annular with active edge), atopic dermatitis (flexural, dry, itch-dominated), rosacea (no scale, no greasiness).
Clearing a resistant case step by step
A 30-year-old man returns for the third time with "dandruff that defeats every shampoo". Work him properly. Step one: confirm the diagnosis — inspect nasolabial folds, eyebrows and presternal chest for the same greasy scale, and scrape the edge for KOH to exclude tinea, which antifungal-shampoo misuse can partially treat and blur. Step two: check he is actually using ketoconazole correctly — applied to the scalp, left five minutes, extended to the face — twice weekly for four weeks, not a cosmetic two-second rinse. Step three: add a short course of hydrocortisone 1% to the face to settle inflammation, planning withdrawal within two weeks. Step four: fix the maintenance schedule — weekly ketoconazole indefinitely interrupted only by long clear spells. Step five: reassess severity — if the disease is unusually extensive, explosive or refractory despite correct therapy, offer HIV testing with counselling, and examine for parkinsonian features in older patients.
The reasoning to articulate: severity itself is a diagnostic sign here. Ordinary seborrhoeic dermatitis is a nuisance; extraordinary seborrhoeic dermatitis is a clue to an immunological or neurological shift, and the two questions (HIV status, neurological examination) cost nothing.
The Indian context
India's heat and humidity thicken the seborrhoeic burden, and monsoon flares are real enough for patients to time their own recurrences. The practical Indian realities: ketoconazole 2% shampoo is cheap and effective, yet patients cycle instead through antiseptic and cosmetic shampoos that contain no antifungal; coal-tar preparations linger in practice with mess but modest evidence; and potent steroid-combination creams bought over the counter produce telangiectatic, steroid-dependent faces that then need unwinding. The HIV link deserves local emphasis — India's testing programme makes the offer straightforward, and marked seborrhoeic dermatitis at a low CD4 count is a recognised presenting feature of advanced HIV in Indian series. In Parkinson disease clinics, seborrhoea is among the most common non-motor skin signs, so a dermatology referral occasionally becomes the first neurological clue.
Frequently asked questions
Which organism underlies seborrhoeic dermatitis?
Malassezia species — commensal yeasts whose lipase-released fatty acids provoke inflammation in susceptible skin rather than causing classical infection.
What is first-line therapy?
Ketoconazole 2% shampoo twice weekly until clear then weekly maintenance, with short mild topical steroid or calcineurin inhibitor for inflamed facial flares.
Why test for HIV in severe seborrhoeic dermatitis?
Explosive, extensive or treatment-refractory disease is a recognised marker of advanced HIV and should trigger counselling and testing.
What is cradle cap?
Yellowish, greasy scale over the infant scalp — a self-limiting neonatal form managed with emollients and dilute antifungal shampoo.
How does seborrhoeic dermatitis differ from psoriasis?
Seborrhoeic disease favours sebum-rich folds with greasy fine scale; psoriasis favours extensor elbows and knees with thick silvery scale and nail pitting.